The Dr. Hyman Show - What Standard Cholesterol Testing Isn't Telling You

Episode Date: December 4, 2023

This episode is brought to you by Rupa University, AG1, and Pendulum.  Dietary cholesterol from saturated fat is often thought to be the cause of high LDL cholesterol and blocked arteries. But we now know from updated research that it’s much more complicated than that. Standard cholesterol testing is outdated because it doesn’t check for particle size and particle number, information that is needed to tell what’s really going on with your cholesterol. Statins are often prescribed to lower LDL cholesterol, but often do not address the root of the problem and can cause very uncomfortable side effects. In today’s episode, I talk with Drs. Elizabeth Boham, Ronald Krauss, and Aseem Malhotra about the true role of cholesterol and what is really behind heart disease. Dr. Elizabeth Boham is a physician and nutritionist who practices Functional Medicine at The UltraWellness Center in Lenox, MA. Through her practice and lecturing she has helped thousands of people achieve their goals of optimum health and wellness. She witnesses the power of nutrition every day in her practice and is committed to training other physicians to utilize nutrition in healing. Dr. Ronald Krauss is a Senior Scientist at Children’s Hospital Oakland Research Institute, a Professor of Medicine at UCSF, and an Adjunct Professor of Nutritional Sciences at UC Berkeley. Dr. Krauss’s research aims to understand how to best prevent cardiovascular disease through early detection and management of its major risk factors: most notably, elevated levels of blood cholesterol and lipoproteins. He has published more than 450 research articles and reviews on metabolic, genetic, dietary, and drug effects on plasma lipoproteins and the risk of coronary artery disease, with more than 100,000 citations of this work. Dr. Aseem Malhotra is an NHS-trained consultant cardiologist and visiting Professor of Evidence-Based Medicine at the Bahiana School of Medicine and Public Health in Salvador, Brazil. He is a founding member of Action on Sugar. In 2015, he became the youngest member to be appointed to the board of trustees of UK health charity The King's Fund. He is a pioneer of the lifestyle medicine movement in the UK and in 2018 was ranked by software company Onalytica as the number one doctor in the world influencing obesity thinking. This episode is brought to you by Rupa University, AG1, and Pendulum. Rupa University is hosting FREE classes and bootcamps for healthcare providers who want to learn more about Functional Medicine testing. Sign up at RupaUniversity.com. Get your daily serving of vitamins, minerals, adaptogens, and more with AG1. Head to DrinkAG1.com/Hyman and get 10 FREE travel packs with your first order. Pendulum is offering listeners 20% off their first month’s subscription of Akkermansia for gut health. Visit PendulumLife.com and use code HYMAN. Full-length episodes of these interviews can be found here: Dr. Elizabeth Boham Dr. Ronald Krauss Dr. Aseem Malhotra

Coming up on this episode of The Doctor's Pharmacy. Let's talk about cholesterol because the test that you get when you go to your doctor is antiquated and it doesn't give you the right information to make a decision about what to do. We live in such an exciting time. We're actively entering a healthcare revolution where consumers want to learn about their body. There are tens of millions of wellness enthusiasts who want to learn about their hormones or gut health, advanced lipids and more. But as a healthcare practitioner, how do you make sure that when a patient walks into your office and says, hey, I really want a Dutch complete or a GI map that you have the right answers and the tools?

Well, Rupa University is the number one educational institute where over 20,000 practitioners a year learn about functional and specialty lab testing. Not only do they have absolutely free live classes hosted every week, but they bring in industry experts to teach in-depth six-week boot camps on all of the most popular functional tests. If you want to level up your knowledge of functional lab tests, make sure to visit rupainiversity.com. It's r-u-p-a-university.com. You know that my goal is to live to be 120 and thrive while doing it. Well, I'm always looking for tools and strategies to help me get there. I want to share with you one of the tools that I found and love, a nutritional supplement called AG1. AG1 supports your body's universal needs like nutrient replenishment, gut optimization, stress management, and immune support. By giving your body nutrients it can easily absorb and utilize, AG1 supports your daily performance

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Heart disease is still the number one killer in the world, yet most people don't actually understand what markers put them most at risk. While cholesterol does play a role in heart health, the most typical testing is outdated and doesn't truly show the full picture. In today's episode, we feature three conversations from the doctor's pharmacy about what cholesterol is and how comprehensive testing can provide

a more complete picture of cardiovascular disease risk. Dr. Hyman speaks with Dr. Elizabeth Boehm about the role of lifestyle and inflammation in heart disease, with Dr. Ronald Cross about the definition of cholesterol and why particle size matters, and with Dr. Asim Malhotra about the use of statins in high cholesterol treatment. Let's jump in. It's estimated that 50% of people in this country and in Europe and 40% worldwide have what's considered elevated cholesterol. And obviously, for those 50% of people, not all of them have to be really concerned about that cholesterol number. It doesn't mean that all 50% of us have to be taking a medication to lower that cholesterol. And so people come in all the time with those questions of, is this cholesterol

too high? And how do I get it down? Do I need to get it down? And the reason we're really looking at cholesterol is because it's one factor that influences somebody's risk of cardiovascular disease, right? I like how you said one factor, not the factor. Exactly. One piece of the puzzle. And for a lot of people, it's not even an important piece of the puzzle, right? But it is one piece of the puzzle, especially for people who have a really high cholesterol, very like familiar hypercholesterolemia.

Genetic. Absolutely. We're talking about LDLs like in the 190s, and we'll talk more about those numbers, total cholesterol in the 300s. You know, there is an association with vascular disease. It can cause plaque buildup, and that can cause, if the plaque is building up around the arteries around the heart, that can cause a heart attack, or in the arteries leading to the brain, it can cause a stroke. So for some people, it's something that's very important. For other people, it's something that's giving us a lot of information

potentially about their health and where do we need to focus. And so I think it's an important thing for us to talk about, like what are all these numbers mean, right? People are so confused. What does this number mean? Do I really need to be worried? So we're going to get deep into all the things you should be thinking about if you want to prevent heart disease, cholesterol being one of them. One of them. And maybe not the most important one, by the way, because two-thirds of people who have heart attacks actually have prediabetes or diabetes, and it's mostly undiagnosed, that 70% of people who come in have pretty good cholesterol, who have heart attacks. About 50% have normal cholesterol.

And, you know, it's really striking that we're kind of like wondering about this condition, which is actually not so cut and dried. And I think I want to get into the numbers. Let's talk about cholesterol. Because in my opinion, and I've written a lot about this, the test that you get when you go to your doctor is antiquated. It's outdated. It's not the cholesterol test you should be getting.

And it doesn't give you the right information to make a decision about what to do. So you typically get your total cholesterol, your triglycerides, your HDL, your LDL. Those are fine. But tell us about what these numbers mean and what cholesterol tests we should be doing that your doctor may not be ordering. And that is available through Quest or LabCorp through your insurance. Absolutely. So when you get your traditional cholesterol panel done, your traditional lipid panel done,

they're giving you the LDL cholesterol, the HDL cholesterol, the total cholesterol. And that's one piece of information, like you said, but we're missing a lot of information there. So it's really important. I love this analogy of the dirt and dump trucks. So dirt and dump trucks. And think of all the dump trucks that are going around carrying dirt. And we can make this analogy with cholesterol. So think of your cholesterol like the dirt.

And the dump trucks are the particles carrying around your cholesterol. So what we're learning is it's not just the amount of dirt somebody has that's important. It's the amount of dump trucks that they have carrying around that dirt. And that the size of the dump trucks are actually really important. And so when you get a typical lipid panel done, you know, you're just finding out the amount of dirt that you have and how much of it is LDL and HDL and triglycerides. And that's important. And we will talk about that, but what's even more important or at least as important, right, is the amount of dump trucks

you have carrying around that dirt. And what we're learning is that or what we've learned is that the the if you have small dump trucks, so if you have a certain amount of dirt, you could either have a few big dump trucks carrying around or a lot of small dump trucks carrying it around. Yeah. And what we're learning is that those small dump trucks, if you have too many small dump trucks carrying it around. Yeah. And what we're learning is that those small dump trucks, if you have too many small dump trucks, that that's actually more concerning, that they can get into the artery lining more, they can cause more plaque buildup, they can get that, that it can help that cholesterol get oxidized through oxidative stress. It's much more dangerous.

So the size of those dump trucks you have carrying around your cholesterol is critically important. Yeah. And something we look at all the time. I mean, the way I think about it is, and another way I kind of look at it is, you know, the number you get on your test is the weight of your cholesterol. So it's milligrams per deciliter. It's just basically the weight. Yep. But it doesn't tell you if that cholesterol is made up of a thousand particles or a hundred particles. So you could have a cholesterol of 150 and it could be 5,000 particles or it could be

500 particles of cholesterol. And that makes a huge difference in your risk of heart disease. And you can't tell from a regular cholesterol test, whether you have a lot of particles or whether they're big particles or small particles. So I think about it sort of like golf balls and beach balls. You know, beach balls are these big, light, fluffy balls that you can bounce and don't hurt anything. And the golf ball is small, but it hits you in the head, it'll knock you out, right? And the golf balls are the things that are the small particles that are dangerous that

bang up against the arteries and cause the plaque to develop and cause heart attacks. So you can't tell that from a regular test. You can have smaller, large LDL, smaller, large HDL, smaller, large triglycerides. And the triglycerides are a little different. It's the big triglycerides that are a problem, not the small ones. But you can really get a sense from these newer tests what's really going on. Because I've seen people with a cholesterol of 300. Their HDLs, which sounds terrible, right?

Because you're supposed to be under 200. Their LDL might be 150, which sounds terrible because it should be under 70. Their HDL is like 110. So they have really high cholesterol. They're skinny, they're healthy, and have diabetes, high blood pressure, they don't smoke, they're older. Often little old ladies have this kind of cholesterol.

There's no evidence that these people are at risk of heart disease because they have large, light, fluffy particles. They might have no small particles, they might have the perfect size and shape of all their cholesterol markers, and their risk is really low. And I remember talking to a colleague, well, more of a mentor, Dr. Peter Libby, who's the chief of cardiovascular medicine at Harvard, who's written the textbook on heart disease at all, cardiology study. And I said, Peter, I have these patients, these little ladies, they cholesterol is 300 and they have this and that. This was like 20 years ago. I'm like, would you treat these people with a statin or a drug? He

said, absolutely not. There's no evidence that these people are at risk, even though their cholesterol is so abnormal. So you can't just go by the cholesterol test that your doctor does. Right. Right? So you need something called what? Like particle size testing. It's telling us about those things that are carrying around your cholesterol. Yeah.

So LabCorp does NMR. Yep. NMR. And Quest does something called Cardio IQ. Yep. Which is similar. And you can ask your doctor for these. And you shouldn't stand for any other test but these these tests. And then they tell you so much. So tell us how do you get a profile that is with

these small, dense, dangerous HDL and LDL? Well, you know, it's interesting. So there's a lot of lifestyle that impacts the size of your LDL particles, right? The size of those, you know, are they small and dense and dangerous or are they big and fluffy and not so dangerous? I mean, there's always a genetic component, right? There's a genetic component, but then there's our lifestyle. And we know that that metabolic syndrome where people are insulin resistant, gaining weight around the belly, they typically have lower HDL. They typically have higher triglycerides, but they also typically have more of these small,

dense LDLs, which are more concerning. And so lifestyle makes a huge impact on the size of those LDL particles. And which part of your lifestyle? What's the biggest thing? The diet. Your diet. What diet causes you to have the dangerous kind of cholesterol?

That sad diet. The standard American diet, right? That's the one that, you know, that full of carbohydrates and sugar and refined and processed foods and lots of alcohol and, you know, simple sugars. It's the starch and sugar that drives it. What does that do to the body that causes these particles? And it actually leads to the high triglycerides, the low HDL, the small particles. Right.

It's that whole process of insulin resistance. And it results in this really unhealthy pattern. And so, you know, we sometimes get clues of that with a standard lipid panel, right? We sometimes get clues when somebody has a low HDL. That's the one, the HDL is the one you want higher. And for men, you want it at least over 40. And for women, at least over 50. And then if that triglycerides are over- I'm like 50 and 60. I'm more aggressive than you. Yeah. Well, that's really true. Like what's optimal, right?

What's optimal, right? If your cholesterol's HDL is 40, probably not optimal. It should be over 50. It really should. It really should. You're right. It's not optimal. I'm a tough customer here. And then the triglycerides, you want at least under 150, or what would you say?

What's optimal? 70. There you go for triglycerides. If your triglycerides are over 100, you're definitely flirting with danger. And there are, you know, there's some genetics involved. And we'll talk about the genetics in a minute. but it is usually a sign of increased carbohydrate load. Like not, and I don't mean broccoli. I mean like flour and sugar. Absolutely. So, you know, you can get some sense of if somebody has,

is prone to metabolic syndrome, insulin resistance with that. But then the particle size testing also gives us a lot of information. The NMR, for example, gives you something called your insulin resistance score. So you can get a sense based on the analysis of the particles of cholesterol that you have, how at risk you are for insulin resistance. So it's just one more piece of the puzzle. And I see people with a cholesterol of 150 who have like 2000,000 particles of LDL, which should be under 1,000, who have like 900 particles of small LDL, which should be under 300 ideally, probably less than 90 is perfect.

And you see that often. And yet their doctor, well, your cholesterol is 150, it's fine. And so you really can get duped by just looking at the total numbers. If it's 300, it might be fine. If it's 150, it might be highly dangerous to you. And it's not so easy without looking at the specific tests. So it's super important. And so what you mentioned is that insulin resistance is the driver of this, which is prediabetes, metabolic syndrome. And to some degree or another, 88% of Americans are metabolically unhealthy and have some degree of this.

50% have prediabetes or type 2 diabetes. Like every other American has diabetes or prediabetes. That's crazy. 75% overweight. And every one of those people is some degree of poor metabolic health. So if this is true, what else does this diet do that accelerates heart disease? Because we now know that it's not just the cholesterol. Like I said, you could have cholesterol 300 and be fine,

but there's a special ingredient you need in order to cause the heart disease. What is that special ingredient? So it's inflammation and oxidative stress, right? So inflammation seems to cause everything these days from depression to cancer to heart disease to diabetes to everything else. So what is the cause of the inflammation in these patients with insulin resistance? So a lot of times, I mean, there's many things, right? But it's our belly fat because we know that that fat around our belly, when we get insulin resistant, we gain more weight around our belly. And we know that visceral fat or weight around the belly, the apple shape is more inflammatory. It secretes all

these inflammatory markers and increases inflammation in the body. And so when people, when we get them to, when they help, when their weight around their belly goes down, when we get that waist-hip ratio better, that inflammation goes down. So basically what you're saying is that fat around your belly is not just holding up your pants, that it's an immunologically active organ. It produces these molecules we call adipose cytokines. You've heard of the cytokine storm with COVID. Well, it's that same chronic cytokine storm that's being released from these fat cells in your belly. They're not just average. I mean, you have fat in your legs or your butt,

it's not gonna do that. These fat cells in your belly are super inflammatory. So then you get the inflammation, which leads to oxidative stress, which then causes what problem with the cholesterol? Right, so when your LDL cholesterol gets oxidized. And what is that? Think of oxidative stress like excessive free radicals or

rusting in the body. But you know, there's, we're always making free radicals when in many different cellular processes in the body, but when there's too many of them, or you don't have enough antioxidants to squelch that oxidate those those free radicals. So if your diet's not rich enough in the polyphenols, or those phytonutrients or your vegetables, then what happens is you get more oxidative stress. And that oxidative stress can shift that LDL cholesterol. And it's that oxidized LDL that's more damaging and more likely to cause plaque buildup and that will lead to heart disease. So it's basically rancid cholesterol in your bloodstream that's the problem, that gets

oxidized, which is like you said, rusting or apple turning brown or your skin wrinkling from too much sun. These are all signs of oxidative. But this happens inside of you and it leads to this inflammatory process, this oxidative stress, and that's what causes the heart disease. And some of the interesting studies I've seen, like the Jupiter study, very big trial from Harvard on heart disease. It's fascinating to me that people had high LDL, but no inflammation, had very low risk.

Yes. People had high inflammation, but kind of okay cholesterol, they were at risk. And those with high cholesterol and high inflammation had the most risk. So I think we have to be focused on inflammation, what's causing that. And it may be that the statin drugs, turns out, the benefits may not have a lot to do with cholesterol lowering. But they're anti-inflammatory. They're very powerful anti-inflammatory drugs, which is, quote, a side effect.

But it actually works. Now there's a lot of better ways to get rid of inflammation besides taking statin drugs. And so, when you're talking about people's cholesterol, you know, how do you decide, you know, what to do for each patient? How do you decide from a functional medicine perspective, you know, how to work these patients up to decide whether that should go on a drug or whether you just do lifestyle? How do you figure that out? I mean, it is a complex process, right, where we're taking a really detailed history and we're looking at more than just those

numbers. We're looking at what are their markers of oxidative stress? You know, we can measure those. We can measure oxidized LDL. We can measure 8-hydroxydeoxyguanosine and lipid peroxides. All of these biomarkers that give us a sense of is there oxidative stress. And by the way, these kinds of tests are not things you'll typically get at your regular doctor. You know, at the Ultra Wellness Center here in Lenox,

Massachusetts, we do functional medicine, which takes a deeper dive into the root causes, into these diagnostic tests, which are not available usually through your traditional doctor. They may not be interested in or know what to do or how to interpret even fasting insulin, which they don't even do. So we really are excited to help people figure out how to look at their risk and design a strategy that's personalized for them using functional medicine. And we see people from all over the world at the Delta Wellness Center doing like Zoom consults now. So it's pretty easy to get access. You know, and it's fascinating because there's so many pieces to

the puzzle. And so when you find somebody with high oxidative stress, you ask that question, why? Why is there high oxidative stress? Is it their poor diet? Is it, you know, inflammation? Is it their microbiome? Is it their microbiome? You know, is it a toxin? Heavy metals. Heavy metals, like a toxin or some other. Pollution. Yes. You know, all the smoke that wildfires in California, that increases risk of cardiovascular disease. Absolutely. Absolutely. So, you know, it's really important to think about all the different things that can lead to oxidative stress and inflammation and then try to tease out what is it for that individual person that we need to focus on. So I think that's important for some people and a lot of Americans. There's so much that's lifestyle related, right? But for some people, their lifestyle is great. And it's more, it's more toxin related that we really need to work on that. Or, or like you mentioned, the microbiome is this is a is an area that's fascinating. We're learning so much about how it influences inflammation in the body.

You know, microbiome in your gut, as well as microbiome in your mouth, right? And gingivitis, and how much that we know, we've known for years that that impacts risk of heart disease because of its inflammatory properties. So those are important things that we need to really investigate and look at. Hey everyone, it's Dr. Mark. A number of years ago, I had a major health crisis. It took me a long time and a lot of trial and error to get my life back together and get back on my feet again. But one of the most important steps to healing I found was increasing my intake of acromantia and fueling my growth of acromantia in my gut. Acromantia is a beneficial bacterial strain that strengthens and regulates the gut lining. It's also one of the most important determinants of maintaining your long-term health, including your weight, your metabolism, so many other things. Back then, I had to find creative

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And now, let's get back to this week's episode of The Doctor's Pharmacy. Cholesterol is a waxy substance that is present in the blood attached to a particle and so cholesterol is also called the lipid so this is a fatty waxy substance that is in all our tissues in the body it's it's an important component of the structure of our cells. It has a lot of important functions in our tissues. But in the blood, when it's attached to lipoproteins, depending on which lipoprotein it's attached to, it can either be associated with higher risk or lower risk. And so the lipoprotein is a particle. It's actually a little round tiny ball containing fat, including cholesterol, but other lipids as well. It can contain triglycerides, which we can talk about as well, in a package surrounded by some proteins. And so it's this lipid protein complex that gives it the name lipoprotein.

That's where the name comes from. And cholesterol is an important part of it, but it's not the only part. And one thing I would just go back to from our earlier discussion is that levels of blood cholesterol do not distinguish individual lipoprotein particles. We measure cholesterol in the blood. It's the sum of all of the cholesterol in all these individual particles and even in the case of LDL, we talked about LDL cholesterol is a bad cholesterol that's the amount of cholesterol on the this little LDL particle but even that doesn't necessarily reflect the the amount of

those particles in the blood and in fact individuals who have this very very prevalent metabolic trait this atherogenic dyslipidemia that you mentioned, very often have normal levels of cholesterol, normal levels of LDL, and that's because the particles, the lipoprotein particles that constitute that triad, surprisingly we discovered, do not have a super large amount of cholesterol. They do have cholesterol as part of the structure of these particles, but there are other features of these small particles, the small LDL in particular, that render them more toxic to the arteries.

There are several things that these particles have on them that cause them to bind to the arteries. There are several things that these particles have on them that cause them to bind to the artery wall more tightly, to be cleared less effectively and removed from the body so they tend to hang around because oxidation of lipids can lead to inflammatory processes which are very important in heart disease. So all of these properties of small LDL are quite different and quite distinct from the cholesterol content. And that's why the cholesterol measurement, while it's a reasonable thing to include in a lipid panel, it does not provide necessarily meaningful information about these particular components.

Yeah, the components that really are much more prevalent in the population than even high cholesterol. Yeah, I mean, I read a study once where I think 75% of people who were admitted to the hospital with a heart attack had normal cholesterol levels. And that's kind of shocking when you think about it. Now, I mean, is it because they're on a statin? I don't know. But I think it sort of speaks to the fact that you can have a horrible profile, but actually, you know, you look okay. So I remember, you know, a patient whose cholesterol was like 150, right?

But their triglycerides were 300 and the HDL was 30. And they have, you know, this terrible profile with small particles. I'm much more worried about someone like that than someone with an LDL, you know, or a cholesterol of 300, but an HDL of 80 or 90 and triglycerides of 50, right? So you kind of don't get the true story. And then doctors just see the LDL being high or 90 and triglycerides of 50, right? So you kinda don't get the true story. And then doctors just see the LDL being high or the total being high and they go, you need statin, instead of actually asking the real question,

which is what's causing the abnormal profile in the first place. Right, in terms of treatment, since you brought up statins, what I'll mention is that even though the small LDL trait is associated with high triglycerides and low HDL, there's really very little evidence, if any, that lowering triglyceride or raising HDL itself has a benefit, whereas lowering of the LDL particles clearly is the central goal of our treatment algorithm. And we certainly use statins when these particles are elevated.

They can work. They're not quite as effective in lowering the small LDL compared with the large LDL, but they can be effective. And so statins still represent something that's relevant if there are high levels of these small particles. And in terms of diet, as you mentioned briefly, one of our other eye-openers was when I started to do dietary studies, I was very interested in nutritional effects and heart disease risk. And I inherited the old paradigm of low fat is good for you, right? Yeah, we all do.

I chaired the American Heart Association Nutrition Committee for a few years, bearing that burden, that mantra. And at the same time, I was doing research in my lab. It showed that when we put people on this low-fat, high-carb diet, we started to induce levels of small LDL. We actually can raise it about 25% of the population. The levels went up. And so that was, to me, a complete paradigm changer.

And I started to try to talk about this. It was not exactly accepted with open arms by our colleagues in nutrition. Putting it mildly. It was heresy. And it took a while. As you say, there's a lag time between discovery and implementation. It took quite a while for the nutrition community and dietary guidelines to start recognizing it, There still is an inordinate focus on carbohydrate can be okay. Saturated fat is bad.

And in terms of saturated fat, I think as you also touched on, we did a number of studies that showed that when you put somebody on a high saturated fat diet, this is fat from dairy and or meat, you did raise the LDL cholesterol level. This has been well established for many years, that the cholesterol level in the LDL does go up when you put them on this high saturated fat diet. But we found that it was almost exclusively in the larger LDL particles, not small particles, which are much less related to risk. So there was kind of a mismatch between the cholesterol reading and the impact on the bad guys, whereas, as you also mentioned, turning it around and putting people on a high carbohydrate diet raise

the small LDL and when we started studying therapies we showed fortunately that if you take people who have a high level of small LDL it's very prevalent trait and put them on a lowrate diet and or had them lose weight. Both of those things are extremely effective in lowering small LDL. There is a genetic component to all of this, which unfortunately some people are struggling with. And diet doesn't always work. Statins don't always do the job. We sometimes have to go to something, you know, more intensive treatments.

Yeah. Well, it's interesting. I mean, sort of, you know, the way I think about it may be very simplistic, but, you know, I think about, you know, different, you know, when you get your cholesterol number, it's measuring the weight of the cholesterol, like milligrams per deciliter. When you're looking at particles, you're looking at the number of the particles and the size of the particles, which is more a qualitative than a quantitative view. And so the way I think about it is that, you know, you could have a cholesterol of like 200, but it could be made up of, you know, 2,000 little BBs or, you know, 100 little beach balls. You know, basically in the beach balls are the big particles that bounce off your arteries. And the BBs are like the small LDl particles that go in and cause heart disease and and i think um you know it's it is it is very

surprising to think about you know the the advice we've been getting for decades about cutting saturated fat increasing carbohydrate even today there's still a big uh you know group of professional societies and dietary recommendations that are, haven't kind of progressed. And, and I think, you know, I sort of want to kind of go back to what you said about saturated fat, because you've published a lot of reviews and papers on the roles of saturated fat and lipids. And in a way, you're a bit of a kind of a black sheep in the cardiology community, because you're, you're saying, wait a minute, the saturated fat may not be as bad as we thought it was. I mean, combining with carbohydrates is bad,

combining with starches and sugars is bad, but instead of butter on your bread may not be good, but butter on your broccoli may be okay. And so when you think about it that way, the question is, do we want to eat saturated fats to raise our size of our LDL, or is it better just to kind of stick with more monounsaturated and just cut the carbohydrates? Like, what's the current thinking about this? Because it's constantly changing. And I also think there's a lot of variation in the population I want to talk about. But for most people, you know, we see suffering from poor metabolic health, which is in part

genetic predisposition, but not genetic predestiny. I mean, in other words, you might have a family history of diabetes, but it doesn't mean you're gonna get it if you follow a healthy lifestyle. Right, right, right. Yeah, let me just touch on that last point,

and then I'll go back to that question. We've done a number of studies in which we varied the carbohydrate content of diets, and also achieved weight loss in various studies and various combinations. What we showed when we published this is that even though there's this very high prevalence of this atherogenic small LDL trait, lipid triad, if you will, the prevalence of that could be reduced down to maybe 5% in the population if you follow a low-carb diet and lose weight. So it's 95% reversible with diet alone.

Now most people don't get that far. And sometimes we can talk about low-carb diets. There's a whole discussion about that. But at least the notion is, as you were saying, that this is not destiny. It's highly manageable with lifestyle. Now, regarding the saturated fat issue, yes I have been sort of, how should I say, kind of poking the bear, if you will, and have generated quite a bit of backlash for some of the things that we published and reported. But there is a fair amount of science behind this and this is the idea. First of all, saturated fat is a nutrient. It's a chemical category consisting of many different types of fats. The other way of

describing it is saturated fatty acids. These are chemicals that have a certain chemical quality that makes them fit into this category of saturated fat. But there's 30 different types of saturated fatty acids. So when we consume, when we talk about saturated fat, it's already incorrect to kind of lump them all together, number one. Number two is saturated fat is not consumed as a substance in itself. Butter may be one of the closest things, but it still is not pure saturated fat. No, it's 60%. Yeah, most of the saturated fat we consume, in fact, just about all of it, is in the context of foods. And so I've been a strong advocate for moving away from this kind of microbe precision

focus on saturated fat to say, well really what we should be thinking about is the overall effects of foods in the diet and they may or may not contain saturated fat, but there are a whole lot of other things to consider when it comes to the nutritional, metabolic, and health effects of foods. So there's two major, actually three major categories of foods that contain relatively high concentrations of saturated fat. There's meat, red meat, and white meat for that matter.

There is dairy, whole fat dairy products, and there are tropical oils. Now these are all different foods, and it's a mistake, I believe, and a growing number of my colleagues, I think, are beginning to believe that it's a mistake to focus on the saturated fat rather than on the food. Because, for example, there is a pretty good body of evidence now that whole fat dairy, maybe not all whole fat dairy, but at least some whole fat dairy products such as yogurt, fermented foods, even cheese, can be associated with heart health benefits that have nothing to do with the saturated fat. There may be an increase in blood cholesterol, but as I said, it's these larger particles which we're less concerned about. And it's these other qualities which we're trying to understand that may have health benefits. So it's a mistake to throw out this particular baby

with a saturated bathwater because we're losing an important nutritional effect that may have significant health benefits. Meats are a bit more complicated. I'm not sure we can say the same thing about meats as having in themselves healthy effects other than the nutrients they contain. Certain nutrients are present in beef that are not present… Dr. Justin Marchegiani Doesn't meat have more stearic acid, which

doesn't have that great of an impact on blood cholesterol? Dr. Peter Salgo Yes, but there are other saturated fats that can raise, I mean, red meat can raise cholesterol, white meat can raise cholesterol, and it's a larger part of us. We published that. But the other question that you raised, I just want to touch on, is should we be trying to increase the size of LDL or make them larger? And I'd have to say that there's really no case to be made for that. Larger LDL particles are less dangerous than the smaller particles, but if you have a whole bunch of them, they can still add up.

They're not completely harmless by any means. And so trying to increase the size of LDL, certainly by taking more, let's say red meat, for example, is not something that I would advocate. So are you saying that meat is a concern when it comes to... Well, it's a more, no, not so much the lipid effects. There's a lot of controversy around this, and I know we could spend a long time talking about the pluses and minuses that are out in the literature. Are there other adverse effects? Does it increase the risk of type 2 diabetes?

Does it increase the risk of cancer? Are we talking about environmental effects that we should be concerned about with the beef industry. I mean, there's all kinds of debate about this. From a health standpoint, we're often, unfortunately, relying on what we call nutritional epidemiology. That is looking at populations and asking them what they eat and then finding out whether they get disease or not. That's a very difficult category of research because you will have a lot of potential for error in making assumptions.

But unfortunately, for most of our dietary recommendations, this approach represents the major basis for making those recommendations. And in the case of red meat, there is a reasonable amount of evidence from these observational studies that raise some concerns. I'm not saying that I'm convinced they're true, but they're out there. Yeah, I mean, it's like, you know, I always say, you know, like, you know, observational studies are like, you know, for example, saying, well, just women over 60 never get pregnant, and women who have sex over 60 never get pregnant. So that means having sex doesn't cause pregnancy. It's like this is kind of essentially how we come up with these observational studies.

There's a correlation, but it does improve causation. So there's a lot of other factors. And with meat, it's like that, you know, a lot of people are eating meat. We're in the studies were during times where we thought meat was bad. And so everybody who was eating meat, you know, what didn't take care of their health. And they actually had way worse confounding factors. They smoked more, they drank more, they ate more, they weighed more, they ate fruits and vegetables, they ate more sugar, processed food, didn't take their vitamins, didn't exercise. So yeah, of course they had more cancer, heart disease and everything else. And when you look at meat eaters and vegetarians who shopped at health food stores, meaning their overall diet quality was better, there was a reduction in risk of death by half in

both the groups, just whether they're eating meat or not. So I think it's complicated. You're right um i want to i want to get back to this test because you know you developed this strategy this test a long long time ago and and i i personally have been using it for 25 plus years uh and now it's more available in a quest and lab core there's different techniques that are used in each lab but you know um can you can you talk about this assay and actually what it's doing and how it works and and and you know why is it why is it different than the typical cholesterol panel and why isn't that good enough you know okay so

uh so first of all there uh there are a couple of uh essays, and I'll discuss each of them. And as you mentioned a few minutes ago, these assays measure the number of particles in the blood, not just LDL, but all the different particles. There's HDL particles and very low-density particles. So it's an entire spectrum of lipoprotein particles are measured, and the units, as you said, are not in milligrams. They are in what we call nanomoles. They're actually a chemical way of defining the number of these particles.

And both of these methods allow analysis of these particle concentrations as a function of their size. So the size of lipoproteins is an important feature of their overall effects, both metabolic and pathologic and that spectrum goes from the smallest particles which are the small HDL through LDL, the next largest particle, and then BLDL and within each of those it separates the different subspecies so we can measure small LDL as part of that spectrum. So that's the overall picture. Now the two methods I'll describe the one that I'm partial to because we invented it. That's a disclosure and part of that disclosure

is that the actual the test was actually patented over 20 years ago and licensed to Quest Diagnostics and so Quest offers it as part of what it calls the CardioIQ panel. There's other tests that can include that, but this is called Lipoprotein Fractionation, and the name of the test is Ion Mobility, I-O-N Mobility. So it's Lipoprotein Fractionation by Ion Mobility. The short name is CardioIQ. So that test actually is still quite remarkable. It takes tiny amounts of blood and squirts it out through a little capillary, and the instrumentation winds up separating each of those particles one by one and spitting them out at the end,

and then they're counted. So each individual particle is counted, and the speed at which it goes through, the time it takes to go through is a function of their size. So it goes from the smallest to the largest particles as you go through the system. So you get this readout, which is really quite detailed. There's more information there than we can actually interpret in the clinic, but there are some key clinical measures that we extract from that, and that is measures of small LDL. We also measure something called medium LDL, which is associated with this.

Those two categories together are the major LDL-related risk factors. We measure large HDL particles. So there's information, and sometimes I think one of the reasons we can talk about why it hasn't been taken up more widely is in some sense there might be too much information for people to try to digest. And I think trying to explain and educate has been part of my mission for all these years. I mean, listen, doctors are smart. That's their job.

Yeah, right, right. But for completeness, I'll just mention the other method, which uses a completely different technique called nuclear magnetic resonance spectroscopy, or NMR. And that test was developed by a company that is now part of LabCorp. And this offers a similar type of readout, although it measures these particles in a very different way. It doesn't actually separate the counts, it creates a signal that is then analyzed, and within that signal, each of these components is identified.

And that's also a widely used test. Well, neither of them are actually widely used, but they're both been taken up, I think, by an increasing number of physicians who are beginning to understand. But it's still a very small minority. So your typical cholesterol test is like a total cholesterol, your LDL, your triglycerides and HDL. That's pretty much it. And we'll talk about some other things that doctors may measure like apo b and a1 but you know the the test you're talking about measures that but it also measures you know whether you have small medium or large ldl it measures the the size of the hdl because that also matters it's not just

the size of the ldl right it measures the size of the triglycerides as well. Yeah, those have less direct impact on heart disease risk. Again, this goes back to the idea that there are three traits that tend to cluster as part of this atherogenic dyslipidemia that we talked about. One is high levels of small LDL. The other is high levels of V LDL. The other is high levels of VLDL, large VLDL particles, which are measured by this technique. And that's more related to triglycerides, right? That's right. You're right. That's where triglyceride is transported primarily. And then there are low levels of the larger HDL particles, which we call HDL2 or HDL2B more technically. And that is a readout of this

test as well. So it can sometimes help to show all three components of that. But the money, if you will, in terms of clinical payoff is mostly related to the small LDL particles. And it measures two things, right? whether you have small and how many there are and how many total particles you have, which also matters, right? Right. So it's both a total number and also the size that matters. Right. Can you explain that? A little bit, yeah. Let's back up and talk about the test you just mentioned, the APOB test, A-P-O-B, capital B, that's a protein that is present in LDL, and it's also present in VLDL. And there's one molecule of APOB in each of these particles. So it turns out conveniently that if one measures APOB in the lab, and this is an easy test to do.

It's not expensive. It's widely available. Not widely done, but widely available. It's widely available, right. It's well standardized, despite some claims to the contrary. It measures the total number of those particles, the LDL and the LDL, and also some particles in between called intermediate density lipoproteins. And so all of that together is a pretty good measure of heart disease risk problems if that test is elevated, because it's usually associated with high levels of small LDL. That's often the major reason that one has high levels

of ApoB. And as I say, there are other particles that may be concerning. Even in the large LDL, there may be some that are not so good, and the BLDL, some that are not so good. So the total ApoB measuring turns out to be a pretty powerful tool for assessing risk. But it doesn't zone in on where that elevation is coming from, as you just mentioned. So from my standpoint, from the standpoint of both evaluation and then treatment, I think it helps me a great deal, and I do this in my practice pretty routinely, is measuring these sub-fractions, including the small LDL than these others. So I know what we're dealing with in a more specific way that we can then target and monitor and see if we can lower, because there are people that show up in my clinic who have high levels of ApoB, but they have high levels of large LDL that are

accounting for that. They do their profiles and they look at their overall risk. There's nothing else wrong. So treating the ApoB, I feel those patients does not necessarily have the rationale that I would use to treat the small LDL because these patients do not seem to carry that same degree of risk, even though the ApoB level is high. I have always had a love-hate relationship with statins

because they are a drug which has some benefits, but what seemed to have happened is that there's been a wholesale embracing of this class of medication as the panacea for preventing and treating heart disease. And your book challenges that thesis. One, that LDL cholesterol is the problem, which is primarily what the statins do is lower LDL. And two, the statins are not a free ride, that they come with a lot of inherent risks and side effects. And three, they're actually not that effective and that the data we have has been highly manipulated. And it reminds me of a quote from, I think, Mark Twain or maybe Roger Williams. He said, there's liars, there's damn liars, and there's statisticians. And I think, you know, the way that the data get squeezed and manipulated often give the impression of a profound benefit. But you challenge that whole hypothesis and you challenge us to think differently about statins.

Before we continue down this track and more detailed discussion, I think what people need to realize is that we are, I am, we are coming from a position about ethical, evidence-based medical practice and about giving the right patient the right treatment at the right time with informed consent and uh and at the same time mark also give people an alternative plan whether or not they choose to take a statin and again that i would always argue that's the the patient's choice ultimately um but also to not be ignoring something that you've pioneered magnificently over many, many years, the impact of lifestyle, which, as you know, is more impactful in many ways than medications and come without side effects.

And mostly, lifestyle has a lot of side effects. Well-being, happiness, joy, good health. All the side effects are good ones. Positive side effects. Better sleep, better sex, weight loss. Yeah, 100%. That's what it's about, right? Because we're all going to die eventually, but we want to have the best chance of having authentic happiness for as long as possible. And of course, our happiness is very much linked to our physical health as well. So this is really the heart of the book. And, you know, I've researched this, as you know, in detail, probably over a decade, looking at cholesterol, trying to understand the

root cause of heart disease, and trying to shift the conversation and shift the balance towards, you know, overall improving individual patients' health, but also population health as well. I think where we've gone wrong is we've grossly, first and foremost, grossly exaggerated the fear of cholesterol in this role of heart disease. Because of that fear, the focus has been that the primary way of preventing heart disease is to reduce cholesterol. The most effective drugs at doing that have been statins, so widely prescribed, Mark. It's estimated potentially about 1 billion people around the world

are prescribed statins. It's also one of the most lucrative drugs in the history of medicine. It's estimated, I think, last year, total revenues from sales of statins have reached a trillion US dollars. So there's a lot of money involved as well, and I think that is important for people to be aware of because think introduces a huge bias into the conversation. A lot of vested interests depend on fear of cholesterol lowering and statins and other cholesterol lowering drugs. So it's like, well, actually, let's just break it down so that people are better informed. And then

one of the things I've also advocated for is something called shared decision making, which is an approach where you have a more equal partnership when it comes to conversations with patients about any kind of treatment or investigation that they're going to go through, but accept that it's really important that we take into consideration patients' individual preferences and values. So if you look at the evidence-based medicine triad, which is geared towards improving patient outcomes, there are three big components. So you'll use your best available evidence, your individual clinical expertise, and last but not least, patient preferences and values. And what I teach

my medical students is if you are adhering to those principles, then you are going to increase your chances of improving your patient's health and well-being. And that's really what it's about. So that's really the background to the book. That's great. You know, I think that's a very important framework. And what I would like to do is zoom out for a minute and have you answer a couple of key questions, because, you know, I hear conflicting versions of the data from cardiologists. And it seems, yes, number one killer in the world is still heart disease. However, I've heard cardiologists say we're winning the war because death rates are going down. We're better at actually treating the disease. We're better at preventing the disease. Statins have played a big role in that. And we shouldn't ignore that

fact. But you suggest that maybe that's not true. And in fact, maybe, you know, that the death rates aren't going down. Maybe heart attack rates aren't going down. So can you kind of unpack the data for us? And what is the truth about, one, you know, this massive drive to put everybody on a statin if your cholesterol is a little high.

Yeah, yeah, absolutely. And the fact that maybe it isn't doing all that it's cracked up to do. So talk about that. Absolutely, Mark. So yeah, that's a very good point, right? So let's try and break all of that down. So death rates from heart disease

started to increase in the 1920s. You know, look at data in the US, let's just look at US data, which pretty much parallels most of Western Europe as well. And it peaked around 1970. And then since 1970, the death rates have started to drop. But you know, something I've published on the BMJ before is to if you break that down to try and see what are the different factors that reduced heart disease, the biggest impact actually was reduction in smoking prevalence probably responsible about 50 percent reduction in death rates other factors emergency care emergency treatment of heart attacks so we had thrombolysis these drugs called thrombolytics that help people we had emergency stenting which

in the acute phase in a heart attack certainly is life-saving not in the stable phase that's a different discussion but certainly in the acute phase um the development of coronary care units so what a lot of people used to die from heart disease um mark because they would suffer uh even once they were in hospital they would have a cardiac arrest which is more likely to happen within 24 48 hours of having a heart attack and uh we we then developed chronic case where we could monitor patients and then defibrillate them they're better at rescuing them from what happens once you get a heart attack. Absolutely.

And in fact, they are life-saving. You know, if you have a cardiac arrest and it's witnessed, then you have, or you're in hospital and it's because of a heart attack, you know, nine times out of 10, you'll be saved from a defibrillator and then you're fine. And your prognosis is the same as somebody that didn't have a cardiac arrest. So all these things are there. Maybe to some degree, the reduction of trans fats in the food supply as well. That also had a role. When you look at statins, and this is something that's actually recently been analyzed. They looked at Western European countries over 12 years, since 2000,

2012, to see had an increase in statin prescription for different risk groups, low risk and high risk. Did that correlate with any reduction in cardiovascular death, death, race, and heart disease? The answer was no. The question is, well, how can that be explained? So again, let's break the data down. If you look at the average increase in life expectancy from taking statins from industry-sponsored data, so we take that with a pinch of salt because industry-sponsored studies, which is most of the statin studies in general are designed and the results are geared to kind of exaggerate the benefits and minimize the harms. But if we take that at face value, okay, even that industry-sponsored-

I want you to stop there for a minute because it's such an important point. Yeah. Most of the data we have on statins is from drug company-funded studies. Yeah. In which they actually often are contracting with research organizations to do the research. They're hiring essentially hit men names to put their name on the study. They design the study, they write up the study, and then they get a bunch of cardiologists to sign off on it. Is that fair to say? Yeah, Mark, absolutely. You're spot on. In

fact, just to take a step back for a second, if you look at the issues around health misinformation, you know, we have something called the health misinformation mess, a quote I take from John Ayanides, professor of medicine at Stanford. And there's something called the seven sins that contribute to misinformed doctors and misinformed unwittingly harmed patients. They're rooted in biased funding of research, right? So research that's funded because it's likely to be profitable, not beneficial for patients, biased reporting in medical journals, biased reporting in the media, biased patient pamphlets, commercial conflicts of interest, defensive medicine, and an inability of doctors

to correctly communicate health statistics to patients and also doctors to not understand health statistics properly. That's something that isn't taught very well at medical school. And it's certainly not something we're encouraged to do. So I've been involved with the BMJ and the medical colleges in the UK in 2015 to try and help revolutionize medical practice through medical education and postgraduate teaching. But it takes time. I mean, I was reading somewhere that when you try and revolutionize or change an approach to something that's been embedded for a very long time within medical practice, apparently it takes 17 years, Mark, before that change happens. So we've got to keep fighting and campaigning for it. But you're right,

this is the issue with statins is not dissimilar to many other drugs. And given that information, given those biases, even if you take all those biases into consideration, best case scenario, there was an analysis done to look at randomized controlled trials of statins in people with heart disease. Forget about prevention for a second. Statins benefits seem to be there much stronger in people who've already had a heart attack or people who've been diagnosed with severe blockages in their arteries. If you look at those people from the trials who took statins religiously every day for about five years, because the trials only tend to last about five years before they're approved and before it changes practice, the average or median increase in life expectancy

is over a five-year period, 4.2 days. So if we accept that slight increase in life expectancy over a five-year period, and then you add in the real world mark, within a few years of statin prescription, even people at high risk of heart disease, at least 50% of those patients stop taking statins within two to three years. You can understand from a scientific perspective, from a data perspective, forget about any fraud or any conspiracy theories, just from the data that's already there, you can explain why statins may have not had any impact on reducing death rates from heart disease in the population. Now, when you look at individuals,

and this is what doesn't often take place in the conversation between doctors and cardiologists and patients, and to be fair and honest on this, I mean, I think most doctors actually don't even know this information. That's another reason I wrote the book is to educate doctors so they can have better discussions with their patients. If you've had a heart attack, and this is, by the way, what I do all the time in my practice. so all my patient letters that go back to general practitioners, all the patients I see, I always put this in there, you know, in the discussion. If you've had a heart attack over a five-year period from an individual, the benefit of a statin taken religiously over five years is it prevents one in 39 of those patients from having a further heart attack, and one in 83

in terms of delaying their death or saving their life right now people who already have had a heart attack or are at very high risk absolutely no we're not talking and by the way for everybody listening 75 of the prescriptions for statins are not for people who have had heart disease or are very high risk. It's for primary prevention. And the data on that is even worse. And I want you to explain that after you kind of unpack the fact that, gee, only one in 83 people have a death prevented.

It means 83 people have to take this drug for five years with all the risks and side effects for one death to be prevented. Yeah. And Matt, so I had a caveat on that. What's interesting is these are also most likely the patients that tolerated the statin and didn't get side effects because those people are somehow weeded out the trials. Often we have something called the pre-randomization running period before a randomized control trial starts where patients who don't tolerate the drug or are

non-compliant, they use this word non-compliant, okay, which doesn't make sense to me because if you're enrolling in a trial and you volunteered, you're likely to be somebody who's enthusiastic about taking a drug, right? So that doesn't make sense to me, but very likely the people with side effects are weeded out within the first few weeks of a trial. And then you then report on the results of the people who tolerated the drug. Okay. So this is still a bias. So I talk to my patients and say, well, it's more likely those 1 in 83 and 1 in 39 figures are people that tolerated the drug and were able to take it for five years. If you add in people who get genuine side effects, and sometimes we don't know whether the side effects they experience are statin or not, and I'll explain what I do with

my patients to kind of weed that out, it's highly likely that that benefit is much smaller if not even potentially non-existent you know we don't really know but there's a chance it is non-existent and and and that's uncertainties and we have to have those discussions with patients i think doctors aren't necessarily very good at saying listen there's a lot of things we don't know but let's just tell you tell you what we do know of course, the potential biases and uncertainties. And Mark, in my experience with all the patients I've had these discussions with, even about talking about industry bias and all that kind of stuff, patients appreciate that. They want honesty from their doctors. Anyway, so that's on the secondary prevention, the high risk. If you look at primary prevention,

and you're absolutely right, Mark, most of the people prescribed statins around the world are not high risk. These are people who have got maybe a slightly high cholesterol or even have a risk profile, more importantly, that suggests they may have, say, a 10% to 20% risk of having a heart attack or stroke in the next 10 years. And there are risk calculators. People can go online and look at those risk calculators. If you have a less than 20% risk, if you're lower risk, you're not high risk from having a heart attack or stroke in the next 10 years, then the statin data suggests approximately, convicting data, 1% benefit. So one in a hundred in preventing a non-fatal heart attack or stroke over five years, but this is crucial. No mortality benefit. You're not going to live one day longer right and when you look at

data and studies looking at when we presented this sort of information to patients in this way and this is without talking about potential side effects not even gone there yet most of those patients mark would choose not to take the pill can you think it's extraordinary so in if we are actually adhering to the principles of ethical, evidence-based medical practice and informed consent, in my view, most people who are prescribed statins around the world would choose probably not to take the pill. I hope you enjoyed today's episode. One of the best ways you can support this podcast is by leaving us a rating and review below. Until next time, thanks for tuning in. Hey everybody, it's Dr. Hyman. Thanks for tuning

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